This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. To examine the effects and adaptive mechanisms (adaptation vs decompensation) of an acute increase in insulin secretory demand (achieved with hemipancreatectomy, HPx ) on the [unreadable]-cell function, in insulin sensitive young female baboons without abnormalities in fasting glucose levels and normal HbA1c. Such increased insulin secretory demand will be created by the hyperglycaemic clamp before and after the HPx. The data obtained will be used as preliminary findings to apply for an RO1 named "Mechanisms of [unreadable]-cell adaptation to stress in baboon and human pancreatic islets" we intend to send to NIH this coming February 1st, 2007.